Article Date: 2/1/2004

diabetes management
Managing Diabetes Medically
Get up to speed on the disease that causes so many ocular problems.
BY DEEPAK GUPTA, O.D., F.A.A.O., Stamford, Conn.

As primary eyecare providers, we're all familiar with the ocular implications of diabetes mellitus, but how much do you know about the disease itself? Let's take the time to learn a little more about this common endocrine disorder.

Diabetes primer

Experts define diabetes as "a group of metabolic diseases characterized by hyperglycemia resulting from defects in insulin secretion, insulin action or both." Ultimately, this disease alters the metabolism of carbohydrates, fats and proteins to cause widespread damage throughout the body.

Here's the physiology of the disease: Two hormones (glucagon and insulin), which are respectively secreted by the alpha and beta cells of the islets of Langerhans of the pancreas, regulate blood glucose levels. Insulin enters the blood stream shortly after a person ingests food, particularly those rich in carbohydrates. When the body needs glucose, insulin facilitates its use to meet the body's needs. Any excess glucose converts to glycogen, which is stored in the liver or muscle, or stores as fatty tissue; the net effect of insulin is to lower blood glucose concentration.

Conversely, the alpha cells of the Islet of Langerhans secrete glucagon during fasting states. The overall effect of glucagon is to elevate blood glucose levels by one of three mechanisms:

1. Glycogenolysis (breakdown of stored glycogen in the liver to make glucose)

2. Gluconeogenesis (conversion of non-glucose substrates into glucose)

3. Glucose sparing (a process in which ketones are formed in the liver).

What's your type?

Diabetes falls into one of two categories: type I and type II. These two main clinical patterns are distinct in terms of etiology, pathogenesis, clinical presentation and treatment.

Type I. Type I diabetes accounts for approximately 10% of all diabetes. Patients who have type I diabetes are typically young, thin and undergo a progressive loss of endogenous insulin leading to hyperglycemia. Professionals used the term "insulin-dependent diabetes" for these patients because of their dependence on insulin administration for survival. The peak incidence is between 10 and 13 years of age.

Physicians often diagnose these patients after they experience an abrupt onset of symptoms. The classic triad of symptoms includes the three Ps:

1. polydipsia (increased thirst)

2. polyphagia (increased hunger)

3. polyuria (increased urination).

These patients are prone to ketoacidosis, a life-threatening complication that results from severe insulin deficiency and can result in diabetic coma and death.

Type II. Type II diabetes is the more common form, accounting for 90% of the total disease population. Two major pathogenetic mechanisms are operative in type II diabetes: impaired islet _-cell function (impaired insulin secretion) and impaired insulin action (insulin resistance or decreased insulin sensitivity). Insulin resistance may be defined as being present whenever normal concentrations of insulin elicit a less-than-normal biologic response. When this patient eats a meal, some insulin secretion still occurs, but at reduced levels.

Patients who have type II diabetes usually aren't dependent on insulin to prevent ketosis or maintenance of life (thus it was called non-insulin-dependent diabetes), but insulin is commonly needed to maintain reasonable blood glucose concentrations.

Type II diabetes typically occurs in people who are older than 40 years, are obese and/or have a family history of diabetes. Unlike type I diabetes, in which the symptoms are pronounced, the onset of type II diabetes is gradual. Doctors often diagnose type II diabetes in asymptomatic patients during routine physical examinations when their laboratory work shows elevated blood glucose levels.

Diagnosing diabetes

Physicians make a definitive diagnosis of diabetes based on any one of the following criteria:

FPG is the most common test. The physician performs this after the patient fasts for at least eight hours, usually in the morning before a patient has breakfast. In this test, the patient ingests a 75 g glucose load dissolved in water and the doctor checks his blood glucose levels after two hours.

Meet the dangers

The chronic complications of diabetes include accelerated vascular disease, neurologic deficits, and other organ-specific degenerative processes. The vascular disease consists of both microangiopathy and macroangiopathy.

Microangiopathy. A disease of the capillaries specifically associated with diabetes. It's characterized by thickening of capillary basement membranes and manifests clinically mostly in the retina and kidney.

Macroangiopathy. An accelerated form of atherosclerotic disease of the arteries that usually manifests clinically in the coronary arteries, cerebral arteries and peripheral vessels of the lower extremities.

Make the treatment specific

Each variation of the disorder has its own approaches to treatment.

Treating type I diabetes. Because patients who have type I diabetes suffer from relative or absolute loss of insulin, these patients require insulin injections. Insulin therapy regimens vary greatly among patients based on their clinical condition, their meal times, exercise schedule and waking/sleeping patterns.

Clinicians generally use one of three therapeutic approaches to insulin therapy:

1. Conventional therapy. This involves one or two daily injections of intermediate-acting insulin alone or in conjunction with rapid-acting insulin.

2. Multiple subcutaneous injections. This technique requires a rapid-acting insulin before each meal and either intermediate or long-acting insulin at bedtime. The advantage is tighter glycemic control than conventional therapy.

3. Continuous subcutaneous insulin infusion. This involves a battery-powered insulin pump to inject insulin into the abdominal wall. A basal rate of insulin infusion occurs throughout the day with additional amounts delivered before each meal. The patient usually checks her glucose level before eating and programs the insulin pump accordingly.

The continuous subcutaneous insulin infusion method provides the tightest glucose control, but also the greatest risk of inducing hypoglycemia (when the blood glucose drops below 70 mg/dL). For more information on insulin, see "Insulin 101," on page 70.


Insulin 101


Insulin falls into one of three basic categories: short-acting, intermediate and long-acting.

1. Short-acting insulin (also called regular insulin) begins to work about five minutes after injection, peaks in one hour, and works for two hours to four hours. Meanwhile, regular insulin (which is still under the short-acting insulin category) reaches the bloodstream in 30 minutes after injection, peaks in two to three hours and lasts from three to six hours.

2. Intermediate-acting insulins reach the bloodstream two to four hours after injection, peak four to 12 hours later and last for approximately 12 to 18 hours.

3. Long-acting insulin reaches the bloodstream six to 10 hours after injection and is effective for 18 to 24 hours. It's often used in combination with a rapid or short-acting insulin as the basal insulin. Insulin mixtures (short or rapid insulin mixed with intermediate-acting insulin) include 70% NPH and 30% regular mixture and a mixture of 50% NPH and 50% regular insulin.

Treating type II diabetes. Although many patients use medications and even insulin, the cornerstone of therapy for type II diabetes is proper nutrition, weight loss and exercise. Patients must attain and maintain ideal body weight, reduce intake of fats, increase intake of high-fiber carbohydrates (e.g., bran, beans, fruits and vegetables), reduce intake of refined sugars and salt and restrict alcohol consumption.

Also, five different oral drug classes are available for the management of type II diabetes.

1. Sulfonylureas. This includes tolbutamide (Orinase), tolazamide (Tolinase), acetohexamide (Dymelor), chlorpropamide (Diabinese) glyburide (Diabeta), Micronase, Glynase), glipizide (Glucotrol, Glucotrol XL) and glimepiride (Amaryl). Sulfonylureas work by binding to receptors on the pancreatic b-cell, causing a cascade of reactions leading to insulin secretion.

2. Meglinitides. The mechanism of action of the two metiglinides, repaglinide (Prandin) and nateglinide (Starlix), is similar to the Sulfonylureas stimulation of pancreatic insulin release. The difference is that meglinitides have a shorter half-life, which results in brief stimulation of insulin release. Patients take these medications at each meal to decrease postprandial blood glucose.

3. Biguanides. Metformin lowers blood glucose primarily by inhibiting hepatic glucose production and secondarily by enhancing peripheral muscle glucose uptake. It also helps to combat insulin resistance, which may help decrease the risk of cardiovascular disease.

4. a-Glucosidase inhibitors. a-Glucosidase enzymes, which are found in the small intestinal epithelium, break down complex starches into oligo- and mono-saccharides and glucose, which are more easily absorbed. The medications, acarbose (Precose) and miglitol (Glycet), inhibit these enzymes that delay carbohydrate absorption. This decreases the postprandial glucose elevation, but has little or no effect on fasting glucose levels.

5. Thiazolidinediones. These work by increasing insulin sensitivity and by increasing glucose use in peripheral tissues, mainly in muscle and fat. Experts don't completely understand their novel mechanism of action, but thiazolidinediones may help suppress glucose synthesis in the liver.

Because these five drug classes work by different mechanisms, many patients are on two or three combinations.

Last but not least

As with any other disease, patient participation is vital in the long-term management of diabetes. Give patients detailed education about nutrition, exercise and the importance of controlling blood glucose levels.

References available on request

Dr. Gupta practices full-scope primary care optometry at Stamford Ophthalmology. You can reach him at


Optometric Management, Issue: February 2004